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To complete translation, replication and movement through cells, a virus relies mostly on the interactions of its genome and encoded-proteins with host factors. Knockouts of specific factors or even subtle changes in their properties can trigger a lack of compatibility in plant-virus interactions and failure of the virus to infect its host. Natural recessive resistance against plant viruses often involves mutations within the host translation initiation factors, which are not detrimental to the host. To understand how these mutations act as resistance genes, it is imperative to know how RNA viruses are translated and what are the key regulatory elements in the viral RNAs.

The broad objective of my research program will be to delve into the mechanistic details of viral translation control, which will be integrated into the larger context of viral replication and plant virus resistance. Of particular interest is the Potyviridaefamily, which encompasses about 30% of the most damaging crop viruses. These RNA viruses pose a curious conundrum on how they are translated. Unlike cellular mRNAs which utilize a 5’ m7(G)ppp(G) cap structure and a 3’ poly(A) tail, the Potyviridaerather contain an internal ribosome entry site (IRES) elements, which recruit the ribosomes at internal positions at close proximity of the initiation AUG rather than entering or scanning from the 5’ end. However, to date, little is known on Potyviridae translational strategies.